VEGF与其受体结合诱导的信号通路在常染色体显性多囊肾病（ADPKD）发生发展中居重要地位。环氧酶-2抑制剂塞来昔布（CXB）可抑制肿瘤细胞VEGFR表达。囊肿上皮细胞具有类肿瘤生长特性。申请人发现CXB减少VEGFR2表达，干扰MAPK通路，通过非COX-2依赖途径抑制增殖。但信号通路的上游如何被调控尚不清楚。我们推测："CXB调控VEGFR2相关转录因子表达，通过上游阻断VEGF/Raf/MAPK通路抑制细胞增殖。" 前期实验采用基因芯片技术已筛选出与VEGFR2密切相关的转录因子HLF、PBX1、Smad3、STAT3和NF-κB1。荧光定量PCR证实CXB能抑制前4种转录因子RNA含量。下一步拟通过体内、外实验进一步观察在CXB处理后转录因子表达量和活性的改变以及与VEGFR2的相互作用。进一步揭示囊肿上皮细胞MAPK信号通路上游VEGFR2的调控机制，发现ADPKD的治疗新靶点。

It is well known that VEGF/VEGFR signal pathway is very important for the regeneration of Autosomal Dominant Polycystic Kidney Disease （ADPKD） . Cyclooxygenase-2 inhibitor celecoxib (CXB) can inhibited VEGFR from a variety of tumor cells. Cyst-lining epithelial cells has the similar characteristic of high proliferation as tumor cells. Our findings provide the first direct evidence that CXB suppresses renal cyst-lining growth in ADPKD, which are chieved by the blockade of binding between VEGF and VEGFR-2.It is still unclear how to regulate upstream of MAPK signal pathway VEGFR-2 expression. Which has becoming the center point of controling signaling pathway.We suppose that CXB could effect transcription factors concerning of VEGFR-2 and interfer VEGF/VEGFR/Raf/ERK/MAPK signaling pathway. By gene chip technology we screened out suitable transcription factors：HLF，PBX1，Smad3，STAT3 and NF-κB1.In front of four transcription factors were detected inhibition of RNA content by realtime fluorescence quantitative PCR. Transcription factors and VEGFR-2 expression would be determined by tests in vitro and in vivo. All these data showed the potent and critically beneficial therapy target on ADPKD.